Protocols for High-Risk Pregnancies. Группа авторов

Figure 7.2 Flow velocity waveform of the umbilical artery and definitions for the different Doppler indices of resistance.

      Cardiac flow velocities

      Normal values and blood flow velocity patterns have been previously reported for cardiac Doppler velocities. More specifically, blood flow velocity values and patterns have been described for the pulmonary and aortic outflow tracts, ductus arteriosus, DV, pulmonary veins, tricuspid and mitral valve, and inferior vena cava. Any fetal structural cardiac abnormality or precordial or postcordial vascular abnormality can affect the blood flow velocity and waveform of the aforementioned vessels and valves. Further discussion of fetal echocardiography is found in Protocol 6.

      Prediction of adverse pregnancy events

      There has been considerable effort over the past two decades with the application of maternal Doppler studies of the uterine arteries in the prediction of adverse pregnancy outcomes including preeclampsia, FGR, fetal demise, and preterm birth. The most distal branches of the uterine artery (spiral arteries) undergo a remarkable transition during the first half of pregnancy, from highly muscularized vessels with high resistance to remodeled vessels with low resistance. This is in response to differentiation of cytotrophoblast to noninvasive and invasive cytotrophoblast, with the latter literally invading and altering spiral artery muscular architecture. It is this change that leads to the enormous blood flow eventually seen in pregnancy (600–800 mL/min).

      There are many publications on the use of uterine artery Doppler for predicting adverse pregnancy outcomes in both low‐risk and high‐risk populations. In the low‐risk population, there does not seem to be a benefit of wide application of this Doppler test as a screening tool for adverse pregnancy events. There may be a role in uterine artery Doppler testing in high‐risk pregnancy as it may identify a subgroup of patients at a higher risk for adverse events, which may lead to useful additional monitoring during pregnancy or preventive strategies. In addition, the high negative predictive value for adverse pregnancy events can provide reassurance. However, before this test can be applied to the general or even the high‐risk pregnancy population, further evidence is needed to elucidate a clear predictive capability, the optimum gestational age for screening, standardization for study technique and abnormal test criteria, and an effective prevention therapy or strategy; this position has been supported by the Society for Maternal‐Fetal Medicine.

      Fetal growth restriction

Blood flow velocity waveforms obtained by pulsed‐wave Doppler velocimetry change in any given fetal vessel across gestation. In the umbilical artery of a normal pregnancy, there is a progressive increase in diastolic flow velocity across gestation, which reflects a decrease in the resistance within the placenta. One characteristic of FGR due to uteroplacental insufficiency is an increase in blood flow resistance within the placenta, which can be detected by Doppler velocimetry upstream in the umbilical arteries. Approximately 40% of cardiac output is directed toward the placenta via the umbilical artery. Thus, as placental disease progresses and blood flow resistance increases, fetal hypoxia may be reflected in the central nervous system (CNS) and the heart is subject to increased workload (afterload). Prior to significant cardiac dysfunction becoming apparent, abnormalities arise in the “prechordial” venous circulation (inferior vena cava, DV, and hepatic veins) in up to 70% of preterm, severely FGR fetuses. Further, recent data from a randomized clinical trial suggest that use of DV to manage early‐onset FGR may reduce long‐term neurodevelopmental delay. Use of Doppler velocimetry in the management of FGR is further discussed in Protocol 41.

      Rh sensitization

      As previously mentioned, fetal anemia resulting from maternal alloimmunization (except anti‐Kell) was historically detected by amniocentesis and assessment of the ΔOD450 and then confirmed by fetal blood sampling. Assessment of the MCA PSV has replaced the ΔOD450 as the gold standard test for fetal anemia. The MCA PSV has greater sensitivity for moderate to severe anemia than does the ΔOD450. Moreover, the ΔOD450 is not useful in Kell sensitization because fetal anemia in this condition is caused by bone marrow suppression rather than hemolysis and thus does not lead to RBC breakdown products in the amniotic fluid normally detected by the ΔOD450.

      One of the resultant pathophysiological features present in Rh disease is a reduction in the viscosity of the fetal blood, which is secondary to a lower hematocrit. This results in an increase in the velocity of blood flow, which can be detected by pulsed‐wave Doppler velocimetry. One of the vessels branching off the circle of Willis is the MCA, which lends itself to interrogation by Doppler because of its location and because the paired middle cerebral arteries carry 80% of the cerebral blood flow. The MCA is first identified with the use of color flow Doppler. With an angle of insonation of 0° (or less than 30° with angle correction), pulse‐wave Doppler velocimetry is used to obtain the flow velocity waveform. From the flow velocity waveform, one can determine the PSV across serial peaks of the systolic component of the flow velocity waveform profile and obtain a mean systolic peak velocity of the MCA flow waveform. Nomograms are available for PSV in the MCA across gestation. Web‐based MCA PSV multiples of the median (MoM) calculators for a given gestational age are also available at perinatology.com.

When the MCA PSV surpasses the threshold of 1.55 MoM, there is a high risk of moderate to severe anemia in the fetus. The original report on this technique for assessing fetal anemia showed that a cut‐off 1.55 MoM has a sensitivity of 100% and a negative predictive value of 100% for moderate to severe anemia. Subsequent studies have shown similar favorable performance characteristics of this screening test. Once this value is surpassed, the fetus can undergo blood sampling to determine the actual fetal hematocrit and determine if a transfusion is necessary. Using Doppler to assess the MCA PSV and identifying anemia in the fetus in this fashion avoids the standard invasive procedural risks of amniocentesis (needed for the ΔOD450) including exacerbation of the Rh sensitization. The MCA PSV measurement has also been used to guide management in cases of anemia due to infections such as parvovirus, loss of a co‐twin in monochorionic pregnancies, and in TAPS.

Management

      Congenital heart disease and arrhythmia

      Several clinical scenarios may warrant fetal echocardiography, which is discussed in more detail in Protocol 6. The ideal time to obtain a fetal echocardiogram is between 18 and 22 weeks of gestation; however, there are several specialized perinatal centers performing this in the first trimester. Counseling and management of the patient with a congenital heart defect involves a variety of steps that include defining the type and severity of cardiac lesion, consideration of the patient’s moral and religious disposition, genetic testing of the fetus (e.g., karyotype, chromosomal microarray, 22Q testing, etc.), and the presence of extracardiac abnormalities. In many instances, one of the most important things to determine in a fetus with congenital heart disease is whether the cardiac lesion will be ductal dependent and require newborn prostaglandin administration to maintain patency of the ductus arteriosus. This is an important step in the management of the pregnant patient, as it will determine whether she needs to be delivered in a hospital with a nursery capable of administering IV prostaglandin.

      Fetal arrhythmias are typically first detected incidentally by routine Doppler auscultation during a prenatal clinic visit or by external electronic fetal monitoring. Further identification of the specific type of arrhythmia